MicroRNA-425 is downregulated in nasopharyngeal carcinoma and regulates tumor cell viability and invasion by targeting hepatoma-derived growth factor Retraction in /10.3892/ol.2024.14245

Zhu,Wenyan; Ma,Yongchi; Zhuang,Xuqin; Jin,Xin

doi:10.3892/ol.2018.8128

MicroRNA-425 is downregulated in nasopharyngeal carcinoma and regulates tumor cell viability and invasion by targeting hepatoma-derived growth factor

Retraction in: /10.3892/ol.2024.14245

Authors:
- Wenyan Zhu
- Yongchi Ma
- Xuqin Zhuang
- Xin Jin
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Affiliations: Department of Otolaryngology-Head and Neck Surgery, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu 223300, P.R. China, Department of Pharmacy, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu 223300, P.R. China
Published online on: February 27, 2018 https://doi.org/10.3892/ol.2018.8128
Pages: 6345-6351
Copyright: © Zhu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Nasopharyngeal carcinoma (NPC), which arises from the nasopharynx epithelium, is most common in Southeast Asia, particularly in Southern China. To date, a variety of microRNAs have been demonstrated to serve key functions in the progression and development of NPC. microRNA‑425 (miR‑425) has previously been reported to be frequently abnormally expressed in a number of different types of human cancer, including lung, gastric, cervical, breast and prostate cancer. However, to the best of our knowledge, the expression patterns, functions and underlying mechanisms of miR‑425 in NPC remain largely unexplored. In the present study, the expression of miR‑425 was revealed to be low in NPC tissues and cell line. Resumption of miR‑425 expression suppressed cell viability and invasion in NPC. Hepatoma‑derived growth factor (HDGF) was identified as a direct target gene of miR‑425 in NPC. HDGF was highly expressed at mRNA and protein levels in NPC tissues. Additionally, HDGF mRNA was negatively correlated with miR‑425 expression in NPC tissues. Furthermore, overexpression of HDGF almost completely rescued the tumor‑suppressing effects of miR‑425 on NPC cell viability and invasion. Taken together, these results demonstrated that miR‑425 acted as a tumor suppressor in NPC by targeting HDGF, suggesting that it may be a novel therapeutic target for the treatments of patients with NPC.

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